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BACKGROUND: Increasing evidences suggest that nonalcoholic fatty liver disease (NAFLD) is associated with neuropsychiatric disorders. Nevertheless, whether there were causal associations between them remained vague. A causal association between neuropsychiatric disorders and NAFLD was investigated in this study. METHODS: We assessed the published genome-wide association study summary statistics for NAFLD, seven mental disorder-related diseases and six central nervous system dysfunction-related diseases. The causal relationships were first assessed using two-sample and multivariable Mendelian randomization (MR). Then, sensitivity analyses were performed, followed by a reverse MR analysis to determine whether reverse causality is possible. Finally, we performed replication analyses and combined the findings from the above studies. RESULTS: Our meta-analysis results showed NAFLD significantly increased the risk of anxiety disorders (OR = 1.016, 95% CI = 1.010-1.021, P value < 0.0001). In addition, major depressive disorder was the potential risk factor for NAFLD (OR = 1.233, 95% CI = 1.063-1.430, P value = 0.006). Multivariable MR analysis showed that the causal effect of major depressive disorder on NAFLD remained significant after considering body mass index, but the association disappeared after adjusting for the effect of waist circumference. Furthermore, other neuropsychiatric disorders and NAFLD were not found to be causally related. CONCLUSIONS: These results implied causal relationships of NAFLD with anxiety disorders and Major Depressive Disorder. This study highlighted the need to recognize and understand the connection between neuropsychiatric disorders and NAFLD to prevent the development of related diseases.

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BACKGROUND: We aimed to investigate the post-cessation T2DM risk in male NAFLD and NAFLD-free smokers in a 7-year cohort study. METHODS: The study population was male adults who underwent annual health checkups in a 7-year cohort study. Recent quitters were categorized into four groups based on their weight gain during follow-up: < 0 kg, 0-1.9 kg, 2.0-3.9 kg, and ≥ 4.0 kg. Cox proportional hazard models, adjusted for various variables, were used to estimate hazard ratios (HRs) for the association between post-cessation weight gain and incident T2DM in NAFLD and NAFLD-free individuals. RESULTS: At baseline, we included 1,409 NAFLD and 5150 NAFLD-free individuals. During a total of 39,259 person-years of follow-up, 222 (15.8%) NAFLD patients and 621 (12.1%) NAFLD-free participants quit smoking, with the corresponding means (standard deviations) of post-cessation weight gain being 2.24 (3.26) kg and 1.15 (3.51) kg, respectively. Among NAFLD individuals, compared to current smokers, the fully adjusted HRs (95% CI) for incident T2DM were 0.41 (0.06-3.01), 2.39 (1.21-4.70), 4.48 (2.63-7.63), and 6.42 (3.68-11.23) for quitters with weight gains < 0 kg, 0.0-1.9 kg, 2.0-3.9 kg, and ≥ 4.0 kg, respectively. For NAFLD-free individuals, we only observed a significant association between post-cessation weight gain ≥ 4.0 kg and the risk of incident T2DM (P < 0.001). Further analysis revealed that the impact of post-cessation weight gain on T2DM risk was not affected by alcohol consumption or obesity status at baseline. CONCLUSIONS: Mild post-cessation weight gain significantly increased the risk of T2DM in male NAFLD patients but not in male NAFLD-free individuals. Therefore, it is recommended that individuals with NAFLD manage their weight after quitting smoking.

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The diagnostic power of the textural features and fractal dimension (FD) for early detection of diabetic retinopathy (DR) were quantitatively evaluated with optical coherence tomography angiography (OCTA). 41 normal healthy OD eyes (age: 46.41 ± 13.69), and 10 diabetic OD eyes (age: 60.90 ± 13.46) in the early stages of DR (mild or moderate non-proliferative diabetic retinopathy (NPDR)) were employed. Four retinal vascular plexuses including nerve fiber layer vascular plexus (NFLVP), superficial vascular plexus (SVP), intermediate capillary plexus (ICP) and deep capillary plexus (DCP) were generated by using OCTA. The FD and the five textural features including contrast, correlation, entropy, energy, and homogeneity in four parafoveal sectors were extracted from OCTA images. The factor of aging on textural features and FD was evaluated based on the comparisons among five normal healthy subgroups. Our results showed that FD in superior sector of NFLVP and in nasal sector of ICP had the significant decreases when comparing the older healthy subgroup (age range: 60-69) with the younger healthy subgroup (age range: 20-29). Our results also indicated that the correlation did not show the significant differences in all sectors of the four retinal sublayers among the normal healthy subgroups except in the temporal sector in NFLVP. Furthermore, our results indicated that the correlation in nasal and inferior sectors in SVP can effectively differentiate diabetic patients in early stages of DR from normal healthy subjects with the highest AUROC values. In our study, the specific textural feature - correlation can effectively stage the early DR, which may contribute to the diagnosis of DR in clinic practice.

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BACKGROUND: With the development of the economy and improvements in living standards, the incidences of diabetes mellitus (DM) and diabetic retinopathy (DR), which is a complication of DM, are on the rise. AIM: To analyze early DR in patients with macular zone changes in biological images using optical coherence tomography angiography. METHODS: A prospective case study was performed on 59 participants: 35 healthy eyes (control group), 35 eyes with diabetes but no DR group (no DR group), and 35 eyes with mild DR (NPDR group). All quantitative comparisons of parameters, including the fovea vascularity area, circularity index, and vascular complexity parameters, were performed using a biological image analysis software. RESULTS: The foveal avascular zone (FAZ) area, FAZ circularity index, number of branches in the area, and the total of the single branches' length in the area was 0.366 ± 0.031, 0.834 ± 0.037, 3241.8 ± 268.3, and 3.860 × 107 ± 0.194 × 107, and 0.421 ± 0.030, 0.739 ± 0.023, 2956.6 ± 476.4, and 3.177 × 107 ± 0.161 × 107 in the no DR group and the NPDR group, respectively, which were significantly different from the corresponding parameters of the control group (P < 0.05). Moreover, there were significant differences between these two groups (P < 0.05). CONCLUSION: This study shows that early microcirculation changes in the macular area of the retina is associated with disease progression. Early changes in DR can be analyzed using optical coherence tomography angiography.

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BACKGROUND: Diabetic retinopathy is severe damage to the retina caused by complications of diabetes, and is the prevailing cause of blindness. Accumulating evidence from both animal models and humans suggests that the inflammatory process plays a key role in the development of diabetic retinopathy and is facilitated by innate immune response. The aim of this study was to examine whether the TLR4 signaling pathway was involved in the streptozotocin-induced diabetic rat retina. METHODS: Diabetes was induced by a single intraperitoneal injection of streptozotocin, and rat diabetic retinopathy was examined at 4 weeks of diabetes duration. Then the accumulated leukocytes were counted in vivo by acridine orange leukocyte fluorography, and the retinal vascular permeability was measured by the Evans blue assay. The expressions of TLR4 and its downstream signaling molecules were measured by RT-PCR or Western blot respectively. To evaluate the effect of blocking TLR4 on diabetic retinopathy, TAK-242, a selective TLR4 antagonist, was administered by intraperitoneal injection. RESULTS: Our results showed that the retina of diabetic rats demonstrated accumulated leukocytes and retinal vascular permeability. The mRNA and protein expressions of TLR4 were upregulated in streptozotocin-treated diabetic rat retina. Furthermore, the protein levels of TLR4 downstream signaling molecules were significantly increased in streptozotocin-treated animals. In addition, the protein levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and interferon (IFN)-ß, three downstream proinflammatory cytokines of TLR4 signal transduction pathway, were also markedly increased in diabetic rats. Administration of TAK-242 attenuated leukocytes accumulated and retinal vascular permeability, and decreased TLR4 downstream signaling molecules and proinflammatory cytokines in streptozotocin-induced animals. CONCLUSIONS: Together, these data have demonstrated that TLR4 has a critical role in streptozotocin-induced diabetic retinopathy at the level of inflammatory cytokine induction, in both the MyD88-dependent and MyD88-independent pathways. TLR4 may become a new potential pharmacological target for treating diabetic retinopathy.

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